Cocaine is a sympathomimetic drug with CNS stimulant and euphoriant properties. High doses can cause panic, schizophrenic-like symptoms, seizures, hyperthermia, hypertension, arrhythmias, stroke, aortic dissection, intestinal ischemia, and MI. Toxicity is managed with supportive care, including IV benzodiazepines (for agitation, hypertension, and seizures) and cooling techniques (for hyperthermia). Withdrawal manifests primarily as depression, difficulty concentrating, and somnolence (cocaine washout syndrome).
Most cocaine users are episodic recreational users. However, about 25% (or more) of users meet criteria for abuse or dependence. Use among adolescents has declined recently. Availability of highly biologically active forms, such as crack cocaine, has worsened the problem of cocaine dependence. Most cocaine in the US is about 45 to 60% pure; it may contain a wide array of fillers, adulterants, and contaminants.
Most cocaine in the US is volatilized and inhaled, but it may be snorted, or injected IV. For inhalation, the powdered hydrochloride salt is converted into a more volatile form, usually by adding NaHCO3, water, and heat. The resultant precipitate (crack cocaine) is volatilized by heating (it is not burned) and inhaled. Onset of effect is quick, and intensity of the high rivals that associated with IV injection. Tolerance to cocaine occurs, and withdrawal from heavy use is characterized by somnolence, difficulty concentrating, increased appetite, and depression. The tendency to continue taking the drug is strong after a period of withdrawal.
Cocaine, an alkaloid present in the leaves of the coca plant, enhances norepinephrine, dopamine, and serotonin activity in the central and peripheral nervous systems.
Enhancement of dopamine activity is the likely cause of the drug’s intended effects and thus of the reinforcement that contributes to developing abuse and dependence.
Norepinephrine activity accounts for the sympathomimetic effects: tachycardia, hypertension, mydriasis, diaphoresis, and hyperthermia.
Cocaine also blocks sodium channels, accounting for its action as a local anesthetic. Cocaine causes vasoconstriction and thus can affect almost any organ. MI, cerebral ischemia and hemorrhage, aortic dissection, intestinal ischemia, and renal ischemia are possible sequelae.
Onset of cocaine’s effects depends on mode of use:
IV injection and smoking: Immediate onset, peak effect after about 3 to 5 min, and duration of about 15 to 20 min
Intranasal use: Onset after about 3 to 5 min, peak effect at 20 to 30 min, and duration of about 45 to 90 min
Oral use: Onset after about 10 min, peak effect at about 60 min, and duration of about 90 min
Because cocaine is such a short-acting drug, heavy users may inject it or smoke it repeatedly every 10 to 15 min.
Effects may differ depending on mode of use. When injected or smoked, cocaine causes hyperstimulation, alertness, euphoria, a sense of increased energy, and feelings of competence and power. The excitation and high are similar to those produced by injecting amphetamines. These feelings are less intense and disruptive in users who snort cocaine powder.
Users who smoke the drug may develop pneumothorax or pneumomediastinum, causing chest pain, dyspnea, or both. Myocardial ischemia due to cocaine use may also cause chest pain (“cocaine chest pain”), but cocaine can also cause chest pain in the absence of myocardial ischemia; the mechanism is unclear. Arrhythmias and conduction abnormalities may occur. Cardiac effects may result in sudden death. Binges, often over several days, lead to an exhaustion syndrome or "washed out" syndrome, involving intense fatigue and need for sleep.
An overdose may cause severe anxiety, panic, agitation, aggression, sleeplessness, hallucinations, paranoid delusions, impaired judgment, tremors, seizures, and delirium. Mydriasis and diaphoresis are apparent, and heart rate and BP are increased. Death may result from MI or arrhythmias.
Severe overdose causes a syndrome of acute psychosis (eg, schizophrenic-like symptoms), hypertension, hyperthermia, rhabdomyolysis, coagulopathy, renal failure, and seizures. Patients with extreme clinical toxicity may, on a genetic basis, have decreased (atypical) serum cholinesterase, an enzyme needed for clearance of cocaine.
Patients who inhale cocaine may develop an acute pulmonary syndrome (crack lung) with fever, hemoptysis, and hypoxia, that may progress to respiratory failure.
The concurrent use of cocaine and alcohol produces a condensation product, cocaethylene, which has stimulant properties and may contribute to toxicity.
Severe toxic effects occur in compulsive heavy users. Myocardial fibrosis, left ventricular hypertrophy, and cardiomyopathy can develop. Rarely, repeated snorting causes nasal septal perforation due to local ischemia. Cognitive impairment, including impaired attention and verbal memory, occurs in some heavy users. Users who inject cocaine are subject to the typical infectious complications.
Diagnosis is usually made clinically. Drug levels are not measured. The cocaine metabolite, benzoylecgonine, is part of most routine urine drug screens.
Treatment of mild cocaine intoxication is generally unnecessary because the drug is extremely short-acting. Benzodiazepines are the preferred initial treatment for most toxic effects, including CNS excitation and seizures, tachycardia, and hypertension. Lorazepam 2 to 3 mg IV q 5 min titrated to effect may be used. High doses and a continuous infusion may be required. Propofol infusion, with mechanical ventilation, may be used for resistant cases.
Hypertension that does not respond to benzodiazepines is treated with IV nitrates (eg, nitroprusside) or phentolamine; beta-blockers are not recommended because they allow continued alpha-adrenergic stimulation.
Hyperthermia can be life threatening and should be managed aggressively with sedation plus evaporative cooling, ice packs, and maintenance of intravascular volume and urine flow with IV normal saline solution.
Phenothiazines lower seizure threshold, and their anticholinergic effects can interfere with cooling; thus, they are not preferred for sedation.
Occasionally, severely agitated patients must be pharmacologically paralyzed and mechanically ventilated to ameliorate acidosis, rhabdomyolysis, or multisystem dysfunction.
Cocaine-related chest pain is evaluated as for any other patient with potential myocardial ischemia or aortic dissection, with chest x-ray, serial ECG, and serum cardiac markers. As discussed, beta-blockers are contraindicated, and benzodiazepines are a first-line drug. If coronary vasodilation is required after benzodiazepines are given, nitrates are used, or phentolamine 1 to 5 mg IV given slowly can be considered.
Heavy users and people who inject the drug IV or smoke it are most likely to become dependent. Light users and people who take the drug nasally or orally are at lower risk of becoming dependent. Stopping sustained use requires considerable assistance, and the depression that may result requires close supervision and treatment.
Many outpatient therapies, including support and self-help groups and cocaine hotlines, exist. Inpatient therapy is used primarily when it is required by physical or mental comorbidity or when outpatient therapy has repeatedly been unsuccessful.
For treatment of infants born to cocaine-addicted mothers, see Prenatal Drug Exposure.